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Mechanisms of Dexamethasone-Induced Hypertension
被引:19
作者:
Ong, Sharon L. H.
[1
]
Zhang, Yi
[1
]
Whitworth, Judith A.
[1
]
机构:
[1] Australian Natl Univ, John Curtin Sch Med Res, High Blood Pressure Res Unit, POB 334, Canberra, ACT 2601, Australia
基金:
英国医学研究理事会;
关键词:
Dexamethasone-induced hypertension;
glucocorticoid;
nitric oxide;
oxidative stress;
pathogenesis;
reactive oxygen species;
D O I:
10.2174/157340209787314315
中图分类号:
R6 [外科学];
学科分类号:
1002 ;
100210 ;
摘要:
Hypertension is a well-recognized complication of excess glucocorticoids, both naturally-occurring and synthetic. Dexamethasone is a potent synthetic glucocorticoid, which has widespread clinical applications. As dexamethasone has purely glucocorticoid activity with negligible mineralocorticoid effects, dexamethasone-induced hypertension (DEX-HT) models have been used for studying the mechanisms of glucocorticoid-induced hypertension. This review examines the characteristics and mechanisms of DEX-HT, both in the human and experimental animal models. The roles of hemodynamics, volume, renin-angiotensin-aldosterone system, sympathetic nervous system, vasodilators including nitric oxide, vasoconstrictors and reactive oxygen species in the pathogenesis of DEX-HT are reviewed and differences from hypertension due to naturally occurring steroids discussed.
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页码:61 / 74
页数:14
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